Ishibashi H, Akaike N
Department of Physiology, Kyushu University Faculty of Medicine, Fukuoka, Japan.
Neuroscience. 1995 Oct;68(4):1139-46. doi: 10.1016/0306-4522(95)00212-2.
The effects of norepinephrine on the low- and high-voltage-activated calcium channels in the neurons acutely dissociated from the nucleus tractus solitarius of 2- to 3-week-old rats were investigated in the nystatin perforated patch recording configuration under voltage-clamp conditions. The norepinephrine had no effect on the low voltage-activated calcium channel but inhibited the high voltage-activated calcium channel in a concentration-, time- and voltage-dependent manner. The norepinephrine slowed the activation phase of the high voltage-activated calcium channel current and the maximum inhibition was 30% of the total current amplitude measured 10 ms after the current activation. The inhibitory effect was eliminated by applying larger depolarizing prepulses. The pretreatment with pertussis toxin completely blocked the norepinephrine effect on high-voltage activated calcium channels, suggesting the contribution of pertussis toxin-sensitive Gi/Go-proteins to the norepinephrine-induced inhibition. Yohimbine but not prazosin nor propranolol antagonized the norepinephrine-induced inhibition, suggesting the involvement of alpha 2-adrenoceptor in norepinephrine-induced inhibition of the high voltage-activated calcium channels. omega-Conotoxin-GVIA, omega-agatoxin-IVA, nicardipine and omega-conotoxin-MVIIC blocked the high voltage-activated calcium channel current by 26, 9, 36 and 11% of the total current respectively, suggesting the existence of N-, P-, L- and Q-type calcium channels in the nucleus tractus solitarii neurons. The current being insensitive to these calcium channel antagonists, termed R-type calcium channel current, also existed. This residual R-type calcium channel was completely blocked by adding 200 microM CD2+. The norepinephrine significantly inhibited N- and P-type calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)
在电压钳制条件下，采用制霉菌素穿孔膜片钳记录模式，研究了去甲肾上腺素对2至3周龄大鼠孤束核急性分离神经元中低电压激活和高电压激活钙通道的影响。去甲肾上腺素对低电压激活钙通道无影响，但以浓度、时间和电压依赖性方式抑制高电压激活钙通道。去甲肾上腺素减慢了高电压激活钙通道电流的激活相，最大抑制作用为电流激活后10毫秒测得的总电流幅度的30%。通过施加更大的去极化预脉冲可消除抑制作用。百日咳毒素预处理完全阻断了去甲肾上腺素对高电压激活钙通道的作用，提示百日咳毒素敏感的Gi/Go蛋白参与了去甲肾上腺素诱导的抑制作用。育亨宾而非哌唑嗪或普萘洛尔拮抗去甲肾上腺素诱导的抑制作用，提示α2肾上腺素能受体参与了去甲肾上腺素诱导的高电压激活钙通道抑制作用。ω-芋螺毒素-GVIA、ω-阿加毒素-IVA、尼卡地平和ω-芋螺毒素-MVIIC分别使高电压激活钙通道电流阻断26%、9%、36%和11%，提示孤束核神经元中存在N型、P型、L型和Q型钙通道。还存在对这些钙通道拮抗剂不敏感的电流，称为R型钙通道电流。加入200μM CD2+可完全阻断这种残余的R型钙通道。去甲肾上腺素显著抑制N型和P型钙通道。（摘要截短于250字）
